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BHS 116.3 Human Physiology and Pathology
Notetaker: Caitlyn McHugh
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Date:05/01/2013, 1st hour
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Reproductive physiology/pathologies
o Process of spermatogenesis
 Hormonal regulation – LH and FSH play role in normal spermatogenesis
o Ovarian cycle
 First half of cycle = follicular phase followed by ovulation followed by the luteal
phase
 Know what happens to ovary during these phases
 Follicular phase
 Developing the follicle
 Two main cell types—outer theca and inner granulosa cells
o Influenced by LH and FSH
 Estrogen production  estrogen is secreted by granulosa cells, fills up
antrum to start growing antrum also released into blood so have systemic
effects as well depending on amount of estrogen in the blood
o Oogenesis is different from spermatogenesis
 First division is right before ovulation second is right after fertilization
o Hormonal regulation of menstrual cycle
 Know regulation of follicular phase leading up to ovulation
 Moderate levels of estrogen are inhibitory to LH and FSH production leading
to decrease in LH FSH production over time, leading to production of single
predominant mature follicle
 Start out with about 6 follicles, only 1 reaches full maturity due to decease in
FSHone with most FSH receptors is the dominant follicle
 Extremely high levels of estrogen triggers LH surge leading to ovulation of mature
follicle
 Positive feedback with high levels of estrogen to trigger this LH surge
o Endometrial cycle
 Various changes in endometrium in same time frame of the follicle know what’s
happening at the same time frame
 i.e. Follicular phase of ovarian cycle corresponds to follicular phase of
endometrium
 Luteal phase of ovarian cycle corresponds to secretory phase of endometrium
 Know various hormone levels occurring at these times
Fertilization and pregnancy
o Capacitation of spermatozoa
o Fertilization reaction/Acrisomal rxn that occurs  allows single spermatozoa to fertilize an
ovum
o Development of blastula that implants into endometrial wall
 Trophoblast cells = cells that actually do implanting into endometriu,
 Inner cell mass develops into fetus
o Once we have implantation of trophoblast cells—blastula has implanted into endometrium
 Trophoblast cells release hCG to help maintain the corpus luteum
 Without hCG corpus luteum – it shrivels into a corpus albicans
BHS 116.3 Human Physiology and Pathology
Notetaker: Caitlyn McHugh
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Date:05/01/2013, 1st hour
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With hCG, corpus luteum remains for first 3 months of pregnancy and is
main source of progesterone and estrogen
After 1st trimester, placenta takes over production of progesterone and
estrogen and hCG levels drop, having shriveling of corpus luteum into
corpus albicans
Corpus luteum needs to be maintained for 1st trimester because primary
source of estrogen and progesterone at this time
Prostate irregularities
o Benign prostatic hyperplasia and prostate cancer
 Know differences between the two
 Various regions of prostate central, transitional and peripheral zones
 2 cell types—stromal cells vs. epithelial cells
Endometriosis
o Presence of endrometrial tissue outside of endometrium
 3 main theories: Regurgitation theory, metaplastic theory and dissemination theory
Preeclampsia and eclampsia
o Know symptoms of both
o When start to have seizures eclampsia
 3 events that occur in eclampsia 
 Placental ischemia
 Improper plavcentation, didn’t develop properly
 Maternal HTN
 Number of reactions going on because of placental ischemia
 Disseminated intravascular coagulation  causes clots that can be dangerous to the
mother
Neoplasia
o Nomenclature
 Benign = -oma
 Malignant = -sarcoma or –carcinoma
 Sarcoma = mesencymal origin
 Carcinoma = epithelial origin
o Cancer incidence vs. cancer death rates
 Prostate and breast = highest incidence
 Lung cancer = highest death rate in both sexes
 Once detect lung cancer, usually advanced
o Benign vs. malignant
 Number of histological differences
 Benign
o well differentiated, resemble tissue from what they originated from
o Grow slowly
o Many times have capsules around them because grow slowly
o Don’t see much local invasion
o No metastases
BHS 116.3 Human Physiology and Pathology
Notetaker: Caitlyn McHugh
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Date:05/01/2013, 1st hour
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Malignant
o cells look nothing like host cells (lack differentiation)
o Fast/slow spurts of growth—varying rates
o Will have local invasion
o metastases
Malignant tumor progression
 Cells found In malignant tumor have various capabilities
 Some are invasive cells, some are metastatic, some cells don’t respond to
growth factor multitude of functionality within the given tumor
 Allows tumor to proliferate and spread
Metastases 2 main phases
 Invade ECM
 Originates in one organ, breaks through basement membrane of organ, get
through extracellular matrix (ECM) to get into blood
 Vascular dissemination phase
 Most of the time immune system gets rid of metastatic cells but those that
survive go to distant target site, must extravasate out of blood and proliferate
into new organ
Oncogenes -- molecular triggers for cancers
 Ras, cyclin D, CDK4
Tumor suppressor genes
 P53 major gene found in a number of cancers
 Retinoblastoma (Rb)
DNA repair gens
 BRCA1 and 2
Apoptotic genes
 Bcl-2
If have DNA damage, can fully repair damage back to normal
 If can’t repair, lead to processes involved in triggering tumor development and
expansion and metastasis of the tumor
Ras = small GTP binding protein
 Mutation in ras that causes it to be oncogenicCan’t hydrolyze GTP and therefore
stays active once active and triggers growth and division of the cell
Cyclins/CDK – cell cycle
 Cyclin binds to CDK to activate CDK acts as a complex
 CDK = kinase that goes to phosphorylate other proteins
 Cyclin D and CDK4  checkpoint between G1 and S phase
 Target = Rb
o In normal state, Rb is hypophosphoylated  only has a few
phosphates attached
 This orientation can bind to E2f to prevent translation i.e.
blocks progression from G1 to S
o When cyclinD-CDk4 is activated, this phosphorylates Rb even
further to have hyperphosphorylation of Rb gene can’t interact
BHS 116.3 Human Physiology and Pathology
Notetaker: Caitlyn McHugh
Date:05/01/2013, 1st hour
Page4
with E2F and therefore can’t block G1 to S so the cell is able to
progress through cell cycle, leading to mitosis and proliferation of
the tumor
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Retinoblastoma tumor
o Familial form
 Have one mutated form of Rb
 Need 2 in order to develop tumor—second mutation occurs from environmental
event
o Sporadic form
 Born with both normal copies of Rb but over time  2 mutations occur from
environmental triggers
P53—molecular policemen
o Whenever there is DNA damage, P53 is activated
o Plays a role in activating other genes
 Activates p21, which puts a halt on the cell cycle to stop progression of cell cycle as
to not propogate damaged DNA
 Activates GAD45 which is a DNA repair gene, cell cycle stops, the GAD45 repairs
damaged DNA
 If this works, repair gene back to normal and regress back to normal
o If GAD45 can’t repair DNA damage = apoptosis of the cell and is no longer to propagate
o If initial DNA damage is so severe and doesn’t warrant attempt at repair—p53 activates
another Bax gene to automatically trigger apoptosis
DNA repair gene – BRCA1 and BRCA2 genes
o Repair damage DNA some thought to regulate transcription of genes like estrogen receptor
Bcl2—inhibits apoptosis
o Bcl2 mutations are associated with lymphomas
o If inhibit apoptosis, prevent cells from dying when DNA is mutated, allows propagation of
mutated DNA in lymphoma cells
Normally ave a nice balance between Bax and BCL2 activation
 If have high Bax activation—a lot of apoptosis
 High Bcl2 –a lot of proliferation
Telomere length
o Telomerase- normally with each cell division, telomere length shortens
o Most cells have a finite number of cell divisions due to telomere length
o Telomerase = enzyme that can relengthen the telomere for a degree during normal cellular
life but normally telomerase becomes inactive and cell reaches point where can no longer
divide
o Stem and germ cells have active telomerase so can divide for much longer periods of time
o Tumor cells = overactive telomerase
 Normal cell that becomes malignant usually has reactivation of
telomeraselengthens telomeres to allow cell to divide many more times resulting in
tumor proliferation